Back to Search Start Over

SARS-CoV-2 variant B.1.617 is resistant to bamlanivimab and evades antibodies induced by infection and vaccination

SARS-CoV-2 variant B.1.617 is resistant to bamlanivimab and evades antibodies induced by infection and vaccination

Authors :
Georg M. N. Behrens
Anna-Sophie Moldenhauer
Hans-Martin Jäck
Sebastian R. Schulz
Stefan Pöhlmann
Heike Hofmann-Winkler
Inga Nehlmeier
Luise Graichen
Markus Hoffmann
Prerna Arora
Amy Kempf
Martin Sebastian Winkler
Anzhalika Sidarovich
Metodi V. Stankov
Nadine Krüger
Source :
Cell Reports
Publication Year :
2021
Publisher :
Elsevier BV, 2021.

Abstract

The emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants threatens efforts to contain the coronavirus disease 2019 (COVID-19) pandemic. The number of COVID-19 cases and deaths in India has risen steeply, and a SARS-CoV-2 variant, B.1.617, is believed to be responsible for many of these cases. The spike protein of B.1.617 harbors two mutations in the receptor binding domain, which interacts with the angiotensin converting enzyme 2 (ACE2) receptor and constitutes the main target of neutralizing antibodies. Therefore, we analyze whether B.1.617 is more adept in entering cells and/or evades antibody responses. B.1.617 enters two of eight cell lines tested with roughly 50% increased efficiency and is equally inhibited by two entry inhibitors. In contrast, B.1.617 is resistant against bamlanivimab, an antibody used for COVID-19 treatment. B.1.617 evades antibodies induced by infection or vaccination, although less so than the B.1.351 variant. Collectively, our study reveals that antibody evasion of B.1.617 may contribute to the rapid spread of this variant.<br />Graphical abstract<br />Between March and May 2021, India reported a steep increase in COVID-19 cases that was linked to SARS-CoV-2 variants, including B.1.617. Hoffmann et al. show that the B.1.617 spike protein mediates robust entry into human cells and evades neutralization by antibodies produced upon infection and vaccination.

Details

ISSN :
22111247
Volume :
36
Database :
OpenAIRE
Journal :
Cell Reports
Accession number :
edsair.doi.dedup.....8a10cde9046f37654a4957880df6edf6
Full Text :
https://doi.org/10.1016/j.celrep.2021.109415